With the advent of “extreme sports” that involve water contact, sport diving, and the increasing number of people engaging in breath-hold diving, a sharp increase in diving injuries has been seen in EDs (Box 133.2). Deaths from breath-hold diving alone have almost doubled in the last 5 years, thus illustrating the potential for injury associated with this form of diving.¹ With acute DCI, rapid assessment and treatment are the foundation of management. Three keys to successful ED treatment are having a high index of suspicion (DCI may have nonspecific findings), performing a thorough neurologic examination, and obtaining hyperbaric medicine consultation when DCI is suspected.

Box 133.2

Fatality Statistics for Diving

Deaths: 120 diving fatalities in the United States and Canada (2007)

Death analyses: men (85%); median age 50 years (men) and 43 years (women)

Obesity: 76% of deaths involved overweight or obese divers

Causes of death: drowning (86%); acute heart condition (9%); arterial gas embolism (3%); decompression sickness (1%)

Activities: 66% of deaths during pleasure of sight-seeing diving

Data from Divers Alert Network. DAN report on decompression illness, diving fatalities and project dive exploration, 2008. Available at www.diversalertnetwork.org/.

Pathophysiology

Dysbarism refers to the effects of variations in ambient (surrounding) pressure on the body. Hypobaric (low-pressure) exposure, such as that experienced by climbers, pilots, and astronauts, can result in symptoms and injuries similar to those found in divers with DCI who are exposed to high pressure while at depth. Decompression injuries during high-pressure (hyperbaric) exposure are far more common.

Diving Physiology

Evaluation of a diver with a water-associated injury requires a basic understanding of diving physiology and the physics of pressure and gases. Different gases have different properties at different depths, which allows gases to be used alone or in combination for different types of diving. The gases of most interest are air, oxygen, nitrogen, helium, and occasionally argon. Deep diving (past 180 feet of sea water [fsw]) often requires helium-oxygen combinations (heliox) to mitigate the effects of nitrogen narcosis (discussed later). Moreover, enriched nitrogen-oxygen combinations (nitrox) may be used to reduce obligations for decompression stops, which is the time spent at more shallow depths to help divers offload the nitrogen built up in the body before exiting a dive.

In general, most recreational divers breathe compressed air and use a self-contained underwater breathing apparatus (SCUBA) when diving to depths of less than 135 fsw. Nitrogen represents about 78% of the gas inhaled with compressed air diving. During diving, hydrostatic pressure “pushes” nitrogen into tissues; nitrogen (an inert gas) then becomes dissolved in plasma and permeates tissues. While at depth, gases remain in solution, and most divers experience minimal difficulty. The deeper that divers travel and the longer that they remain at depth, the more saturated the blood and tissues become with nitrogen (or other inspired inert gases). One of the tenets of diving is to ascend slowly when resurfacing. Doing so allows the dissolved (inert) gases to escape the tissues slowly and be cleared via normal respiration. If a person ascends to the surface too quickly, the dissolved gases come out of solution and form bubbles in tissues or within the vasculature. When these bubbles are not cleared by the lungs (“blown off”) they can embolize and cause downstream injury or they can cause local damage at the site of formation (autochthonous bubbles). When bubbles cause symptoms, the disorder is called DCI. Depending on the size, number, and location of the bubbles, DCI has a wide range of manifestations, from pain (most common symptom), numbness, and fatigue to severe neurologic symptoms such as seizure, paralysis, and loss of consciousness (LOC).

Bubble Physiology

Knowledge of bubble mechanics and the effects of bubbles in various tissues is critical to understanding the pathophysiology and treatment of DCI. Venous bubbles are not usually problematic because the lungs can filter large gas loads. Bubbles have damaging effects when they remain within tissues or embolize. Bubbles can pass from the venous circulation to the arterial circulation via a right-to-left shunt (patent foramen ovale or arteriovenous malformation). Bubbles can grow from “nucleation sites” within body tissues, such as the joint spaces, tendon sheaths, periarticular sheaths, and peripheral nerves.² Once inside these areas, bubbles can act as emboli and block perfusion of distal tissues or act as foreign bodies with resultant vascular damage through activation of the inflammatory and clotting cascades. Interestingly, scientists are now evaluating a possible biologic marker of DCI. As gas emboli within the circulation induce decompression stress, endothelial cells release microparticles in response to cellular activation or cell death. These microparticles may, in the future, reflect a biologic marker of decompression stress that can be used to gauge the extent of disease, efficacy of treatment, or prophylaxis.³

Principles of Gas Laws and Dysbarism

An understanding of the pertinent diving gas laws, units of measurement, abbreviations, and mathematic conversions helps facilitate the treatment and disposition of dive-injured patients. At sea level, the pressure of the atmosphere on the body (ambient pressure) is 760 mm Hg, which equals 1 atm. The term for the absolute pressure on a diver at sea level is called atmospheres absolute (ATA), and it represents the total sum of the pressure on a diver. Therefore, at sea level, a dive computer gauge reads zero, but sea level also represents one surrounding atmosphere of pressure (1 ATA). This knowledge helps the physician better comprehend the circumstances surrounding a dive injury. Although there are a large number of gas laws, the two that are the most important in diving medicine are Boyle’s law and Dalton’s law.

Boyle’s Law

Boyle’s law aids in understanding why a diver needs to exhale while ascending from depth. According to Boyle’s law, the volume of a quantity of gas (V) varies inversely with the pressure on that gas (P) if it is kept at a constant temperature. It is often represented by the following formula:

where the subscripts 1 and 2 indicate two different combinations of pressure and volume; in other words, the product of pressure and volume will always remain a constant.

Usually, as a diver descends deeper, the surrounding pressure increases in linear fashion. Water pressure at the surface is referenced as 1 ATA. In general, for every 33 fsw that the diver descends, there is an increase in pressure of 1 ATA. Therefore, a descent to 33 fsw would equal 2 ATA, a descent to 66 fsw would equal 3 ATA, and so on. Furthermore, for the first 33 fsw descended, the volume of gas present is reduced by half the original amount of gas at the surface. At 66 fsw, the volume is one third the original volume. The greatest changes in volume occur closest to the water surface and represent a significant vulnerability to injury (Fig. 133.1).

Fig. 133.1 Boyle’s law.

ATA, Atmospheres absolute.

Dalton’s Law

Dalton’s law of partial pressures is critical to understanding the mechanisms for DCS, nitrogen narcosis, and oxygen toxicity. It is represented by the formula

where P_total is the total pressure of the gases that a diver breathes and the subscripts 1, 2, and 3 indicate the partial pressure of each individual gas. This law explains why the effects of the individual gases increase as a diver travels deeper during a dive. Put simply, as a diver descends, the amount of each gas inhaled increases proportionally with increasing depth. When diving with air tanks, divers are exposed to higher partial pressures of both oxygen and nitrogen the farther down that they travel. Importantly, nitrogen at high concentrations has a narcotic effect (nitrogen narcosis), and oxygen at high concentrations can be toxic (oxygen toxicity). Both problems are described in further detail later in the chapter.

Presenting Signs and Symptoms

Barotrauma

Barotrauma is sustained from failure to equalize the pressure of an air-containing space with that of the surrounding environment. The most common examples of barotrauma occur during air travel and scuba diving.^1,⁴ Barotrauma occurs only in gas-containing (compressible) body spaces. More than 95% of the body is composed of water (incompressible). Typical gas-filled spaces include the sinuses, middle and inner ears, air-filled areas within carious or filled teeth, and hollow viscous organs such as the intestines and lungs. Barotrauma incurred during descent is called a “squeeze.” Barotrauma incurred during ascent is called a “reverse squeeze,” “reverse block,” or expansion injury.

Differential Diagnosis and Medical Decision Making

Table 133.1 lists the differential diagnosis for dive injuries based on the time of onset of symptoms.

Table 133.1 Differential Diagnosis of Dive Injuries Based on the Onset of Symptoms

SYMPTOM ONSET	INJURIES TO CONSIDER
Descent	Ear or sinus barotrauma Inner ear barotrauma

Bottom

Nitrogen narcosis

Oxygen toxicity

Trauma

Ascent 15 min after resurfacing

Arterial gas embolism

15 min to 24 hr after resurfacing

Decompression sickness

Ear Barotrauma

With an intact tympanic membrane (TM), the only communication for equilibration of pressure between the middle ear and the ambient atmosphere is through the eustachian tube (ET).⁵ Divers typically perform Valsalva maneuvers during decent to equalize pressure in the middle ear. Failure to equalize leads to pain and damage from injury to the middle or inner ear and results in TM edema, rupture, or hemorrhage, as well as rupture of the oval or round window (may lead to a perilymphatic fistula).⁵ Table 133.2 summarizes the types of ear barotrauma.

Table 133.2 Barotrauma of the Ear

External Ear Barotrauma (“Squeeze”)

During diving, water replaces the air in the external ear canal. Obstructions such as wax, a bony growth, or earplugs can create an unvented air space that changes in volume in response to changes in ambient pressure. During descent, the increased pressure “squeezes” this space and causes the TM to bulge outward toward the canal with resultant pain, small hemorrhages, or TM blebs.⁴ Prevention consists of cleaning the external canal and removing any foreign bodies.

Middle Ear Barotrauma (“Squeeze”)

Middle ear barotrauma (middle ear squeeze, barotitis media) is the most common disorder in divers and hyperbaric medicine patients. It usually occurs during descent as a result of an inability to equalize pressure across the TM. It occurs in 30% of novice divers and 10% of experienced divers.⁶ When water exerts pressure on the external TM and pushes it inward, a diver can usually equalize the pressure in the ears by swallowing, yawning, performing a Valsalva maneuver, or blowing against closed nostrils. Divers are often unable to clear their ears because of anatomic variability of the ET, inflammation, a viral infection, or upper aerodigestive dysfunction. Without equalization of the pressure, the TM ruptures. As little as 100 mm Hg (5 fsw) can create a pressure differential large enough to rupture the TM.⁷ Symptoms of middle ear barotrauma are ear pain, pressure, and muffled hearing. If the TM is ruptured, vertigo may occur because of the effects of cold water on the middle ear or TM. Treatment consists of decongestants, rest from diving, and follow-up with an otorhinolaryngologist (refractory cases). In general, these injuries are self-limited. However, if a patient needs hyperbaric medicine treatments, pressure equalization tubes may be placed to prevent middle ear barotrauma. Any form of TM rupture, placement of a pressure equalization tube, or myringotomy would be a contraindication to wet water diving because water comes in direct contact with the middle ear.

Subcutaneous Emphysema

Pneumothorax

Pneumothorax is a severe, potentially life-threatening pulmonary overpressure syndrome. Rupture allows bubbles and gas to enter the pleural space, which can place pressure on the lung itself. Symptoms vary greatly, depending the volume of air entering the pleural space and the patient’s baseline lung function. Patients may have simple dyspnea or exhibit shock or life-threatening cardiac arrest (tension pneumothorax). The most common symptoms are sharp chest pain, shortness of breath, and occasionally a sudden, dry, hacking cough. Pain may also be felt in the shoulder, neck, or abdomen. Treatment is immediate administration of high-flow oxygen and possible needle decompression or tube thoracostomy (or both). If pneumothorax occurs during hyperbaric treatment or surface decompression table treatment, immediate venting of the pneumothorax (Heimlich valve) may be necessary to prevent the development of tension pneumothorax.

Arterial Gas Embolism

AGE, the most lethal result of pulmonary barotrauma, is a common cause of death in recreational divers.⁸ Its incidence is underestimated because many in-water deaths are classified as drowning. When rupture of the lung parenchyma leads to intravascular bubbles, these bubbles can embolize and cause end-organ damage. Sadly, this disorder is often seen in inexperienced divers who panic at depth and shoot to the surface without exhaling slowly. The symptoms are dramatic, usually LOC immediately or within minutes of the diver reaching the surface. Death is common. The arterial emboli are most deadly when they travel to the coronary or cerebral circulation. Cerebral AGE is manifested very much like a stroke and results in headache, confusion, agitation, hemiplegia, or sudden LOC. Air embolism can also block blood flow through the coronary circulation and lead to cardiac ischemia, dysrhythmias, shock, and death.

Definitive treatment of AGE consists of high-flow oxygen on site and immediate hyperbaric recompression. The sooner patients are recompressed, the less likely they are to have permanent neurologic injury. Full recovery is common when recompression is available immediately. It is important to remember that AGE can occur in shallow water while breathing compressed gas or during breath-hold diving. This is in contrast to DCS, which usually occurs following a deep or prolonged dive when high nitrogen partial pressure develops.⁹ AGE also occurs in the hospital setting as a result of iatrogenic errors (central line manipulation, hemodialysis), but it can occur with any procedure or trauma that can entrain gas into the bloodstream.

Gastrointestinal Barotrauma

The stomach and intestine are both air-filled organs and, though rarely affected, are susceptible to barotrauma. Specifically, gas expansion occurring on ascent can cause nausea, belching, flatulence, mild stomach pain, and reflux. These symptoms resolve fairly quickly after the diver resurfaces because these spaces are typically easily vented.

Tooth Barotrauma

The small air pockets that exist in teeth and under fillings are susceptible to barotrauma (barodontalgia). Most people experience pain only on ascent, but tooth fractures have occurred (odontocrixis). Decompressions as mild as those experienced during commercial air flight pressurization (8000 feet or 0.75 ATA) are sufficient to cause barodontalgia. Such patients should be referred for dental evaluation, and divers should make their dentists aware of their diving hobby so that air pockets can be avoided.

Decompression Sickness

DCS, or “the bends,” is a type of DCI that usually occurs after diving at deeper depths. In accordance with Dalton’s law, tissues become highly permeated with inspired inert gases with increasing depth. DCS can also occur after long shallow dives if significant tissue saturation has occurred. It can cause a spectrum of symptoms. Diagnosis can be difficult because divers may complain of only mild to moderate symptoms, which they tend to ignore or attribute to other causes. Frequently, a diver complains, “I just don’t feel right,” or has limb pain without trauma that is assumed to be muscular in origin. DCS symptoms rarely develop while the diver is in the water. The key to diagnosing dive-related injuries is to (1) elicit the timing of the onset of symptoms (before, during, or after a dive), (2) determine the presence of any dive-related DCS risk factors (dehydration, alcohol use, inexperience, failure to follow the decompression tables, flying after diving, reverse-profile diving, multiple dives per day, decompression diving, smoking, advanced age, cold water, patent foramen ovale, and obesity), and (3) have a low threshold for suspicion of DCS when symptoms develop. DCS is classically divided into three types according to the severity of illness and the location of symptoms. In reality, DCS symptoms overlap and the basic treatment is usually the same for all types—recompression with hyperbaric oxygen.

Type I (“Mild” Symptoms)

Type I DCS describes mild symptoms such as joint pain (most common), dermatologic manifestations, and lymphatic-associated swelling and edema as a result of the effects of gas bubbles in the tissues (Box 133.3). Bubble formation in joints is due to the greater negative pressure that exists in the joint spaces.¹⁰ Pain is most often felt in the shoulders or knees but can appear in any joint. The pain is gradual and aching and varies in intensity, usually worsening with time. Limb pain in divers affects the upper extremities three times more often than the lower extremities, and its distribution is often asymmetric.¹¹ Caisson workers, however, are affected more often in their lower limbs.⁸ Merritt makes the point that type I DCS usually involves pain in the extremities whereas type II DCS usually involves central structures.⁷

Box 133.3

Type I Decompression Sickness

Musculoskeletal Pain (“Limb Bends”)

Most common manifestation of DCS

Dull, aching pain often in the shoulder or knee

Pain occurring both at rest and with movement

No evidence of joint inflammation on examination

Occurs within 24 hours of resurfacing but almost never at depth and rarely within the first few minutes after surfacing

Cutaneous DCS (“Skin Bends”)

Itching and pruritus most common symptoms (self-resolving)

Cutis marmorata (mottled appearance of the skin)

Peau d’orange (rindlike skin seen in the truncal area)

“Fleas” (formication-like symptoms of insects on the skin)

Lymphatic Effects and Edema

Swelling in the soft tissues or in areas of lymph nodes

Usually localized

Very uncommon

Definitive Treatment

Definitive treatment is recompression

All patients require oxygen. Remember to consult a hyperbaric medicine specialist early if the patient is being brought from a dive accident

DCS, Decompression sickness.

Adapted from Bove AA, Davis J. Bove and Davis’ diving medicine. 4th ed. Philadelphia: Saunders; 2004; and U.S. Department of Commerce: NOAA navy diving manual. 5th ed. Flagstaff, Ariz: Best Publishing; 2005.

Dermatologic DCI (“skin bends”) can have several manifestations. A diver can experience itching alone (without a rash) in localized or generalized areas of the arms, legs, face, or trunk (“fleas”). This form is commonly thought to follow dry dives, appears shortly after resurfacing, and lasts only a few minutes to a few hours.¹² Other dermatologic manifestations of DCS are mottling (cutis marmorata) and rindlike skin (peau d’orange).

Type II (“Severe” Symptoms)

Type II DCS causes more severe symptoms that have a high risk of leading to major disability or death. Cardiopulmonary, neurologic, and inner ear manifestations predominate (Box 133.4). All patients with type II DCS symptoms require emergency recompression in a hyperbaric chamber. The sooner they are recompressed, the more likely they are to have a full recovery. However, even if treatment is delayed several days, recompression can still be helpful. Multiple treatments may be necessary to maximize recovery.

Box 133.4 Type II Decompression Sickness

Type II is associated with a higher risk for permanent disability or death than type I.